The effect of SARS coronavirus on blood system: its clinical findings and the pathophysiologic hypothesis.
Identifieur interne : 005D44 ( Main/Exploration ); précédent : 005D43; suivant : 005D45The effect of SARS coronavirus on blood system: its clinical findings and the pathophysiologic hypothesis.
Auteurs : Mo Yang [République populaire de Chine] ; Kam-Lun E. Hon ; Karen Li ; Tai-Fai Fok ; Chi-Kong LiSource :
- Zhongguo shi yan xue ye xue za zhi [ 1009-2137 ] ; 2003.
Descripteurs français
- KwdFr :
- Adulte, Antigènes CD (immunologie), Antigènes de différenciation (immunologie), Enfant, Humains, Hématopoïèse (physiologie), Hémopathies (immunologie), Hémopathies (physiopathologie), Molécules d'adhérence cellulaire, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (physiopathologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS.
- MESH :
- immunologie : Antigènes CD, Antigènes de différenciation, Hémopathies, Syndrome respiratoire aigu sévère.
- physiologie : Hématopoïèse.
- physiopathologie : Hémopathies, Syndrome respiratoire aigu sévère.
- virologie : Syndrome respiratoire aigu sévère.
- Adulte, Enfant, Humains, Molécules d'adhérence cellulaire, Virus du SRAS.
English descriptors
- KwdEn :
- Adult, Antigens, CD (immunology), Antigens, Differentiation (immunology), CD13 Antigens (immunology), Cell Adhesion Molecules, Child, Hematologic Diseases (immunology), Hematologic Diseases (physiopathology), Hematopoiesis (physiology), Humans, SARS Virus, Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (physiopathology), Severe Acute Respiratory Syndrome (virology).
- MESH :
- chemical , immunology : Antigens, CD, Antigens, Differentiation, CD13 Antigens.
- immunology : Hematologic Diseases, Severe Acute Respiratory Syndrome.
- physiology : Hematopoiesis.
- physiopathology : Hematologic Diseases, Severe Acute Respiratory Syndrome.
- virology : Severe Acute Respiratory Syndrome.
- Adult, Cell Adhesion Molecules, Child, Humans, SARS Virus.
Abstract
Severe acute respiratory syndrome (SARS) has recently recognized as a new human infectious disease. A novel coronavirus was identified as the causative agent of SARS. This report summarizes the hematological findings in SARS patients and proposes a hypothesis for the pathophysiology of SARS coronavirus related abnormal hematopoiesis. Hematological changes in patients with SARS were common and included lymphopenia (68% - 90% of adults; 100% of children, n = 10), thrombocytopenia (20% - 45% of adults, 50% of children), and leukopenia (20% - 34% of adults, 70% of children). The possible mechanisms of this coronavirus on blood system may include (1) directly infect blood cells and bone marrow stromal cells via CD13 or CD66a; and/or (2) induce auto-antibodies and immune complexes to damage these cells. In addition, lung damage in SARS patients may also play a role on inducing thrombocytopenia by (1) increasing the consumption of platelets/megakaryocytes; and/or (2) reducing the production of platelets in the lungs. Since the most common hematological changes in SARS patients were lymphopenia and immunodeficiency. We postulate that hematopoietic growth factors such as G-CSF, by mobilizing endogenous blood stem cells and endogenous cytokines, could become a hematological treatment for SARS patients, which may enhance the immune system against these virus.
PubMed: 12844398
Affiliations:
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Hon</name></author><author><name sortKey="Li, Karen" sort="Li, Karen" uniqKey="Li K" first="Karen" last="Li">Karen Li</name></author><author><name sortKey="Fok, Tai Fai" sort="Fok, Tai Fai" uniqKey="Fok T" first="Tai-Fai" last="Fok">Tai-Fai Fok</name></author><author><name sortKey="Li, Chi Kong" sort="Li, Chi Kong" uniqKey="Li C" first="Chi-Kong" last="Li">Chi-Kong Li</name></author></analytic><series><title level="j">Zhongguo shi yan xue ye xue za zhi</title><idno type="ISSN">1009-2137</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Antigens, CD (immunology)</term><term>Antigens, Differentiation (immunology)</term><term>CD13 Antigens (immunology)</term><term>Cell Adhesion Molecules</term><term>Child</term><term>Hematologic Diseases (immunology)</term><term>Hematologic Diseases (physiopathology)</term><term>Hematopoiesis (physiology)</term><term>Humans</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (physiopathology)</term><term>Severe Acute Respiratory Syndrome (virology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte</term><term>Antigènes CD (immunologie)</term><term>Antigènes de différenciation (immunologie)</term><term>Enfant</term><term>Humains</term><term>Hématopoïèse (physiologie)</term><term>Hémopathies (immunologie)</term><term>Hémopathies (physiopathologie)</term><term>Molécules d'adhérence cellulaire</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Syndrome respiratoire aigu sévère (physiopathologie)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antigens, CD</term><term>Antigens, Differentiation</term><term>CD13 Antigens</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Antigènes CD</term><term>Antigènes de différenciation</term><term>Hémopathies</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Hematologic Diseases</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Hématopoïèse</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Hematopoiesis</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Hémopathies</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hematologic Diseases</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Cell Adhesion Molecules</term><term>Child</term><term>Humans</term><term>SARS Virus</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Enfant</term><term>Humains</term><term>Molécules d'adhérence cellulaire</term><term>Virus du SRAS</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) has recently recognized as a new human infectious disease. A novel coronavirus was identified as the causative agent of SARS. This report summarizes the hematological findings in SARS patients and proposes a hypothesis for the pathophysiology of SARS coronavirus related abnormal hematopoiesis. Hematological changes in patients with SARS were common and included lymphopenia (68% - 90% of adults; 100% of children, n = 10), thrombocytopenia (20% - 45% of adults, 50% of children), and leukopenia (20% - 34% of adults, 70% of children). The possible mechanisms of this coronavirus on blood system may include (1) directly infect blood cells and bone marrow stromal cells via CD13 or CD66a; and/or (2) induce auto-antibodies and immune complexes to damage these cells. In addition, lung damage in SARS patients may also play a role on inducing thrombocytopenia by (1) increasing the consumption of platelets/megakaryocytes; and/or (2) reducing the production of platelets in the lungs. Since the most common hematological changes in SARS patients were lymphopenia and immunodeficiency. We postulate that hematopoietic growth factors such as G-CSF, by mobilizing endogenous blood stem cells and endogenous cytokines, could become a hematological treatment for SARS patients, which may enhance the immune system against these virus.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Sha Tin</li></settlement><orgName><li>Université chinoise de Hong Kong</li></orgName></list><tree><noCountry><name sortKey="Fok, Tai Fai" sort="Fok, Tai Fai" uniqKey="Fok T" first="Tai-Fai" last="Fok">Tai-Fai Fok</name><name sortKey="Hon, Kam Lun E" sort="Hon, Kam Lun E" uniqKey="Hon K" first="Kam-Lun E" last="Hon">Kam-Lun E. Hon</name><name sortKey="Li, Chi Kong" sort="Li, Chi Kong" uniqKey="Li C" first="Chi-Kong" last="Li">Chi-Kong Li</name><name sortKey="Li, Karen" sort="Li, Karen" uniqKey="Li K" first="Karen" last="Li">Karen Li</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Yang, Mo" sort="Yang, Mo" uniqKey="Yang M" first="Mo" last="Yang">Mo Yang</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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